2. Cell Cycle/DNA Damage Epigenetics Apoptosis Autophagy
  3. HDAC Apoptosis Autophagy
  4. Quisinostat

Quisinostat  (Synonyms: JNJ-26481585)

目录号: HY-15433 纯度: 98.34%
COA 产品使用指南

摩尔计算器

Quisinostat (JNJ-26481585) 是一种高效的，第二代，具有口服活性的 pan-HDAC 抑制剂 (HDACi)，对 HDAC1、HDAC2、HDAC4、HDAC10、HDAC11 作用的 IC50 值范围为 0.11-0.64 nM。Quisinostat 具有广泛的抗肿瘤活性。Quisinostat 在成神经细胞瘤中能诱导自噬 (autophagy)

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Quisinostat Chemical Structure

Quisinostat Chemical Structure

CAS No. : 875320-29-9

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     可免费申领三个不同产品的试用装。

3.  试用装只面向终端客户。

规格 价格 是否有货 数量
10 mM * 1 mL in DMSO ￥1320
In-stock
2 mg ￥600
In-stock
5 mg ￥1200
In-stock
10 mg ￥1800
In-stock
50 mg ￥4300
In-stock
100 mg 现货 询价
200 mg   询价  
500 mg   询价  

* Please select Quantity before adding items.

Customer Review

Other Forms of Quisinostat:

Quisinostat 相关抗体

Top Publications Citing Use of Products

查看 HDAC 亚型特异性产品:

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HDAC HDAC1 HDAC2 HDAC3 HDAC4 HDAC5 HDAC6 HDAC7 HDAC8 HDAC9 HDAC10 HDAC11 HD1 HD2

  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

Quisinostat (JNJ-26481585) is a potent, second-generation and orally active pan-HDAC inhibitor (HDACi), with IC50 values ranging from 0.11 nM to 0.64 nM for HDAC1, HDAC2, HDAC4, HDAC10 and HDAC11. Quisinostat has a broad spectrum antitumoral activity[1]. Quisinostat can induce autophagy in neuroblastoma cells[2].

IC50 & Target[1]

HDAC1

0.11 nM (IC50)

HDAC2

0.33 nM (IC50)

HDAC4

0.64 nM (IC50)

HDAC10

0.46 nM (IC50)

HDAC11

0.37 nM (IC50)

HDAC3

4.86 nM (IC50)

HDAC5

3.69 nM (IC50)

HDAC8

4.26 nM (IC50)

HDAC9

32.1 nM (IC50)

HDAC6

76.8 nM (IC50)

HDAC7

119 nM (IC50)

细胞效力
(Cellular Effect)
Cell Line Type Value Description References
D283 Med IC50
< 200 nM
Compound: Quisinostat
Antiproliferative activity against human D283 Med cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay
Antiproliferative activity against human D283 Med cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay
[PMID: 33636537]
Daoy IC50
< 100 nM
Compound: Quisinostat
Antiproliferative activity against human Daoy cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay
Antiproliferative activity against human Daoy cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay
[PMID: 33636537]
HEK-293T IC50
0.06 μM
Compound: Qui
Cytotoxicity against HEK293T cells incubated for 72 hrs by CCK-8 assay
Cytotoxicity against HEK293T cells incubated for 72 hrs by CCK-8 assay
[PMID: 35175762]
HepG2 IC50
0.03 μM
Compound: Qui
Cytotoxicity against human HepG2 cells incubated for 72 hrs by CCK-8 assay
Cytotoxicity against human HepG2 cells incubated for 72 hrs by CCK-8 assay
[PMID: 35175762]
HuT78 EC50
6.5 nM
Compound: 3
Pro-apoptotic activity in human HUT78 cells after 18 hrs by caspase-Glo 3/7 assay
Pro-apoptotic activity in human HUT78 cells after 18 hrs by caspase-Glo 3/7 assay
[PMID: 30122227]
Sf9 IC50
0.000617 μM
Compound: JNJ-26481585
Inhibition of recombinant full length human HDAC1 expressed in baculovirus infected Sf9 cells using FAM-RHKK-Ac as substrate incubated for 17 hrs by electrophoretic mobility shift assay
Inhibition of recombinant full length human HDAC1 expressed in baculovirus infected Sf9 cells using FAM-RHKK-Ac as substrate incubated for 17 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.00196 μM
Compound: JNJ-26481585
Inhibition of recombinant full length human HDAC10 expressed in baculovirus infected Sf9 cells using FAM-RHKK-Ac as substrate incubated for 17 hrs by electrophoretic mobility shift assay
Inhibition of recombinant full length human HDAC10 expressed in baculovirus infected Sf9 cells using FAM-RHKK-Ac as substrate incubated for 17 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.00216 μM
Compound: JNJ-26481585
Inhibition of recombinant full length human HDAC2 expressed in baculovirus infected Sf9 cells using FAM-RHKK-Ac as substrate incubated for 17 hrs by electrophoretic mobility shift assay
Inhibition of recombinant full length human HDAC2 expressed in baculovirus infected Sf9 cells using FAM-RHKK-Ac as substrate incubated for 17 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.00404 μM
Compound: JNJ-26481585
Inhibition of recombinant full length human HDAC7 expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 3 hrs by electrophoretic mobility shift assay
Inhibition of recombinant full length human HDAC7 expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 3 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.00461 μM
Compound: JNJ-26481585
Inhibition of recombinant full length human HDAC4 expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 1.5 hrs by electrophoretic mobility shift assay
Inhibition of recombinant full length human HDAC4 expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 1.5 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.00595 μM
Compound: JNJ-26481585
Inhibition of recombinant full length human HDAC5 expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 3 hrs by electrophoretic mobility shift assay
Inhibition of recombinant full length human HDAC5 expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 3 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.0067 μM
Compound: JNJ-26481585
Inhibition of recombinant human HDAC9 (604-1066 residues) expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 3 hrs by electrophoretic mobility shift assay
Inhibition of recombinant human HDAC9 (604-1066 residues) expressed in baculovirus infected Sf9 cells using FAM-RHKK-TFAc as substrate incubated for 3 hrs by electrophoretic mobility shift assay
[PMID: 31938464]
Sf9 IC50
0.11 nM
Compound: 6
Inhibition of full length recombinant human HDAC1 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
Inhibition of full length recombinant human HDAC1 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
[PMID: 27606546]
Sf9 IC50
0.33 nM
Compound: 6
Inhibition of full length recombinant human HDAC2 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
Inhibition of full length recombinant human HDAC2 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
[PMID: 27606546]
Sf9 IC50
4.86 nM
Compound: 6
Inhibition of full length recombinant human HDAC3/NCOR2 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
Inhibition of full length recombinant human HDAC3/NCOR2 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
[PMID: 27606546]
Sf9 IC50
76.8 nM
Compound: 6
Inhibition of full length recombinant human HDAC6 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
Inhibition of full length recombinant human HDAC6 expressed in baculovirus infected Sf9 cells using RHKK-Ac as substrate by fluorescence analysis
[PMID: 27606546]
体外研究
(In Vitro)

Quisinostat inhibits HDAC isozymes in vitro[1].
? Quisinostat (30-1000 nM; 24 hours) is a potent pan-HDAC inhibitor in tumor cells[1].
? Quisinostat has a broad spectrum antiproliferative activity against solid and hematologic cancer cell lines and induces apoptosis[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Quisinostat 相关抗体:

Western Blot Analysis[1]

Cell Line: Human A2780 ovarian carcinoma cells
Concentration: 30 nM, 100 nM, 300 nM, 1000 nM
Incubation Time: 24 hours
Result: Induced H3 and H4 acetylation at concentrations as low as 30 to 100 nM.
体内研究
(In Vivo)

Quisinostat (40 mg/kg; p.o.; once daily; for 3 days) acts as a potent HDAC1 inhibitor that inhibits p21waf1,cip1 ZsGreen tumors in vivo[1].
? Quisinostat induces continuous H3 acetylation in tumor tissue in vivo[1].
? Quisinostat (10 mg/kg; once daily; i.p.; for 14 days) strongly inhibits the growth of large pre-established HCT116 colon xenografts[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: NMRI nude mice, with HCT116 colon carcinoma cells xenografts[1]
Dosage: 10 mg/kg
Administration: Intraperitoneal injection, once daily, for 14 days
Result: Strongly inhibited the growth of large pre-established HCT116 colon xenografts.
Clinical Trial
分子量

394.47

Formula

C21H26N6O2
CAS 号
性状

固体

颜色

Off-white to yellow

运输条件

Room temperature in continental US; may vary elsewhere.
储存方式
Powder -20°C 3 years
In solvent -80°C 6 months
-20°C 1 month
溶解性数据
细胞实验： 

DMSO 中的溶解度 : 41.67 mg/mL (105.64 mM; 超声助溶 (<60°C); 吸湿的 DMSO 对产品的溶解度有显著影响，请使用新开封的 DMSO)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.5350 mL 12.6752 mL 25.3505 mL
5 mM 0.5070 mL 2.5350 mL 5.0701 mL
查看完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。

  • 摩尔计算器

  • 稀释计算器

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

质量
=
浓度
×
体积
×
分子量 *

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

浓度 (start)

C1

×
体积 (start)

V1

=
浓度 (final)

C2

×
体积 (final)

V2

动物实验：

请根据您的 实验动物和给药方式 选择适当的溶解方案。

以下溶解方案都请先按照 In Vitro 方式配制澄清的储备液，再依次添加助溶剂：
——为保证实验结果的可靠性，澄清的储备液可以根据储存条件，适当保存；体内实验的工作液，建议您现用现配，当天使用；
以下溶剂前显示的百分比是指该溶剂在您配制终溶液中的体积占比；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的方式助溶

  • 方案 一

    请依序添加每种溶剂： 10% DMSO    40% PEG300    5% Tween-80    45% Saline

    Solubility: ≥ 2.5 mg/mL (6.34 mM); 澄清溶液

    此方案可获得 ≥ 2.5 mg/mL（饱和度未知）的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀；再向上述体系中加入 50 μL Tween-80，混合均匀；然后再继续加入 450 μL 生理盐水 定容至 1 mL。

    生理盐水的配制：将 0.9 g 氯化钠，溶解于 ddH₂O 并定容至 100 mL，可以得到澄清透明的生理盐水溶液。
  • 方案 二

    请依序添加每种溶剂： 10% DMSO    90% (20% SBE-β-CD in Saline)

    Solubility: ≥ 2.5 mg/mL (6.34 mM); 澄清溶液

    此方案可获得 ≥ 2.5 mg/mL（饱和度未知）的澄清溶液。

    以 1 mL 工作液为例，取 100 μL 25.0 mg/mL 的澄清 DMSO 储备液加到 900 μL 20% 的 SBE-β-CD 生理盐水水溶液 中，混合均匀。

    2 g SBE-β-CD（磺丁基醚 β-环糊精）粉末定容于 10 mL 的生理盐水中，完全溶解至澄清透明。
动物溶解方案计算器
请输入动物实验的基本信息：

给药剂量

mg/kg

动物的平均体重

g

每只动物的给药体积

μL

动物数量

只
由于实验过程有损耗，建议您多配一只动物的量
请输入您的动物体内配方组成：
%
DMSO +
% 
+
%
Tween-80 +
%
Saline
如果您的动物是免疫缺陷鼠或者体弱鼠，建议 DMSO 中的在最后工作液体系中的占比尽量不超过 2%。
方案所需 助溶剂 包括：DMSO， ，均可在 MCE 网站选购。 ，Tween 80，均可在 MCE 网站选购。
计算结果
工作液所需浓度 : mg/mL
储备液配制方法 : mg 药物溶于 μL  DMSO（母液浓度为 mg/mL）。
您所需的储备液浓度超过该产品的实测溶解度，以下方案仅供参考，如有需要，请与 MCE 中国技术支持联系。
动物实验体内工作液的配制方法 : 取 μL DMSO 储备液，加入 μL 。 μL ，混合均匀至澄清，再加 μL Tween 80，混合均匀至澄清，再加 μL 生理盐水。
连续给药周期超过半月以上，请谨慎选择该方案。
请确保第一步储备液溶解至澄清状态，从左到右依次添加助溶剂。您可采用超声加热 （超声清洗仪，建议频次 20-40 kHz），涡旋吹打等方式辅助溶解。
纯度 & 产品资料

纯度: 98.34%

COA (171 KB) HNMR (291 KB) RP-HPLC (250 KB) MS (71 KB)

产品使用指南 (1538 KB)
参考文献

Quisinostat 相关分类

完整储备液配制表

* 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month。-80°C储存时，请在6个月内使用，-20°C储存时，请在1个月内使用。

可选溶剂 浓度 溶剂体积 质量 1 mg 5 mg 10 mg 25 mg
DMSO 1 mM 2.5350 mL 12.6752 mL 25.3505 mL 63.3762 mL
5 mM 0.5070 mL 2.5350 mL 5.0701 mL 12.6752 mL
10 mM 0.2535 mL 1.2675 mL 2.5350 mL 6.3376 mL
15 mM 0.1690 mL 0.8450 mL 1.6900 mL 4.2251 mL
20 mM 0.1268 mL 0.6338 mL 1.2675 mL 3.1688 mL
25 mM 0.1014 mL 0.5070 mL 1.0140 mL 2.5350 mL
30 mM 0.0845 mL 0.4225 mL 0.8450 mL 2.1125 mL
40 mM 0.0634 mL 0.3169 mL 0.6338 mL 1.5844 mL
50 mM 0.0507 mL 0.2535 mL 0.5070 mL 1.2675 mL
60 mM 0.0423 mL 0.2113 mL 0.4225 mL 1.0563 mL
80 mM 0.0317 mL 0.1584 mL 0.3169 mL 0.7922 mL
100 mM 0.0254 mL 0.1268 mL 0.2535 mL 0.6338 mL
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Quisinostat875320-29-9JNJ-26481585JNJ26481585JNJ 26481585HDACApoptosisAutophagyHistone deacetylaseshistonedeacetylasehematologicmalignanciesInhibitorinhibitorinhibit

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